GRAND RAPIDS, Mich. (WOOD) — A research team at the Van Andel Institute in Grand Rapids says it has found distinct physiological and molecular differences in obese people that could be used to determine an increased risk for certain diseases or more precise treatment.
The findings were published Monday in the medical journal Nature Metabolism. The study found ties between insulin and obesity and was able to draw distinct lines using DNA to establish if someone was more likely to be obese and/or more likely to be at risk for certain diseases.
The field of science here is called epigenetics. Dr. J. Andrew Pospisilik, the chair of VAI’s Department of Epigenetics, describes it as how DNA presents itself.
“If the DNA is the instructions of who we are, we can obviously modulate that a little bit by having a bit tighter packaging or a bit loosening of the DNA. That means certain genes might get expressed a little bit more or less. So it can enhance or optimize or make worse what the genetic blueprint says,” Pospisilik told News 8.
He compares it to how worker bees create a new queen.
“We know that environment triggers a queen bee to be the queen bee. She’s fed the royal jelly,” Pospisilik said. “So there’s a little bit of a dietary stimulation and then the whole body takes this different trajectory. That kind of interaction could be taking place here. That’s going to be the focus of future studies.”
One of the big mysteries of human biology is UPV — unexplained phenotypic variation. Most experts believe the mystery of UPV lies in epigenetics and could be key to offering more precise medical treatment and a starting point for preventing for certain diseases.
“You could think of (UPV) as unexpected variability,” Pospisilik said. “We all know identical twins. Unexpected phenotypic variation would be if two identical twins aren’t really that identical. It’s unexpected that they’re not identical. They should be. Their genes are the same. They grew up in the same environment. Why didn’t they come out the same? And that’s UPV — the why not. So we think we found one major molecular axis that controls how variable the gene environment blueprint can be.”
The obesity study analyzed mice along with data from TwinsUK, a research resource including genetic maps of identical twins from the United Kingdom. The researchers found four metabolic subtypes: two prone to leanness and two prone to obesity. In people prone to obesity, one group showed a noticeable pattern that the VAI team claims is due to that epigenetic trigger: they show higher lean muscle mass along with higher fat, plus higher-than-normal inflammatory signals and high insulin levels.
“I like to think of it as a rugby player phenotype, like big, plenty of muscle mass, plenty of mass everywhere, but also plenty of (fat),” Pospisilik said. “Whereas there’s, you know we might poke fun at ourselves in science, there’s the desk job where you’ll gain some fat mass, but you have less muscle mass than the next person.”
One of the surprising finds was that in the subtype with high levels of muscle mass, the levels of insulin were higher than expected.
“For the obesity research world, that’s massive, because (common thought) says that insulin goes up after obesity because obesity causes a person to have too much insulin. But this data implied — and the (data from the) mice prove it — that insulin is causing the disease,” Pospisilik explained. “Insulin is a growth hormone, so it causes you to store your fuels. So, it makes sense that obesity could be caused by insulin.”